Dementia, including Alzheimer's disease, remains one of the biggest global public health challenges facing our generation. In fact, as the average age of the world population goes up, the incidence and prevalence of this terribly-debilitating disease is rising. Specifically, the population of those with dementia is expected to triple in approximately 10-15 years.
So far, dementia has resisted all attempts to slow down cognitive and functional progressive impairments, and stymied all efforts to help affected people from all walks of life recover from its ravages. In addition to the significant personal impact of this disease, dementia has an immense (and growing) world-wide societal impact. Although its true financial impact is impossible to measure (and is certainly underestimated), the costs of dementia in the United States already exceeds one percent of the global gross domestic product (GDP).
Stage 1-2 dementia is typically referred to as mild cognitive impairment (MCI) or vascular cognitive impairment (VCI). Experimental studies (mainly involving animals) have been conducted to assess the role of glutamate and medical research on both animals and humans. These studies show that mentally stimulating activities are related to measurable improvements in brain vascular health, and in both brain structure (i.e. neurogenesis) and function (i.e., formation and reactivity of synapses). More importantly, neuroscience research demonstrates that when neural binding occurs (primarily through novel learning approaches) neurons release Glutamate, an excitatory neurotransmitter. This neurotransmitter, among other things, signals to the rest of the brain to decrease the amount of cortical atrophy. Although a certain amount of cortical atrophy does occur during the aging cycle, individuals with dementia do experience an unnaturally steep and progressive acceleration of atrophy secondary to glutamate loss. Persistent and targeted new learning approaches are essential to prevent the steep deceleration of cortical shrinkage.
Cognitive intervention occurs when subjects initiate multiple novel learning sessions, which promote neural binding and the release of glutamate, and serve to decrease the progression of cortical atrophy. This process involves mentally stimulating a cognitively impaired individual (i.e., brain exercises for a sick brain) to help grow new brain connections and limit the progression of functional and neurocognitive impairments with are inherent in dementia. Research has shown that not just any brain exercises will suffice. Specifically, brain exercises that are new and novel are required. Too many existing “brain games” fail by convincing our seniors that something they have down repeatedly (e.g., bridge, crossword puzzles) will be beneficial in decreasing the extent of their dementia. This approach is not based on current clinical science.
What is needed is a system and method for cognitive intervention for patients with early-stage dementia; more particularly, a system and method that assesses and enhances the cognitive capabilities of patients that have been diagnosed with dementia in the earliest stages (i.e., Stages 1-2), and prevent the onset/lessen the progression of neurocognitive decline. The present invention fulfills these needs as well as other needs.